CELLULITIS AND ERYSIPELAS

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Literature review current through: Dec 2016. | This topic last updated: Jan 12, 2017.

INTRODUCTION — Cellulitis and erysipelas are skin infections that develop as a result of bacterial entry via
breaches in the skin barrier [1]. Cellulitis and erysipelas manifest as areas of skin erythema, edema, and
warmth. They differ in that erysipelas involves the upper dermis and superficial lymphatics, whereas cellulitis
involves the deeper dermis and subcutaneous fat.

The clinical manifestations, diagnosis, microbiology, and treatment of cellulitis and erysipelas will be reviewed
here. Issues related to special forms of cellulitis are discussed separately. EPIDEMIOLOGY — The incidence
is about 200 cases per 100,000 patient-years [2]. Cellulitis is observed most frequently among middle-aged
individuals and older adults, while erysipelas occurs in young children and older adults [3,4].

Predisposing factors include disruption to the skin barrier as a result of trauma (such as insect bites,
abrasions, penetrating wounds, or injection drug use), inflammation (such as eczema or radiation therapy),
preexisting skin infection (such as impetigo or tinea pedis), varicella, and edema (due to venous insufficiency)
[5,6]. Lymphatic obstruction following surgical procedures also predisposes to cellulitis. Such procedures
include saphenous venectomy, breast cancer axillary node dissection, and lymph node dissection for pelvic
malignancy [7-11]. Breaks in the skin between the toes ("toe web intertrigo") are perhaps the most important
potential sites for pathogen entry [5,12]. However, breaches in the skin may be small and clinically inapparent.

MICROBIOLOGY — The vast majority of cases of erysipelas are caused by beta-hemolytic streptococci
[4,13-15].

The most common cellulitis pathogens are beta-hemolytic streptococci (groups A, B, C, G, and F) and S.
aureus, including methicillin-resistant strains (methicillin-resistant S. aureus); gram-negative aerobic bacilli are
identified in a minority of cases [12-14,16-20]. A prospective study of nonpurulent (eg, nonculturable) cellulitis
among 179 hospitalized patients found that beta-hemolytic streptococci accounted for 73 percent of cases
(diagnosed by positive blood culture results or serologic testing for anti-streptolysin-O and anti-DNase-B
antibodies); despite the lack of an identifiable etiology in 27 percent of cases, the overall clinical response rate
to beta-lactam therapy was 96 percent [21].

Less common pathogens include H. influenzae (buccal cellulitis), clostridia and non-spore-forming anaerobes
(crepitant cellulitis), pneumococcus, and meningococcus [22-28]. In immunocompromised patients, the
spectrum of potential pathogens is much broader, and infectious disease consultation is warranted.

Cellulitis pathogens implicated in special clinical circumstances discussed in detail separately include:

●Pasteurella multocida and Capnocytophaga canimorsus (see "Soft tissue infections due to dog and cat
bites" and "Initial management of animal and human bites")
●Aeromonas hydrophila and Vibrio vulnificus (see "Soft tissue infections following water exposure")
●S. aureus (see "Orbital cellulitis")
●S. pneumoniae (see "Orbital cellulitis")
●Streptococcus agalactiae (see "Cellulitis following pelvic lymph node dissection", section on
'Streptococcal sex syndrome')
●Streptococcus iniae (see "Fever and rash in the immunocompetent patient")
●Clostridium species (see "Clostridial myonecrosis")

whereas cellulitis involves the deeper dermis and subcutaneous fat. prior to the conjugate vaccine era. erysipelas has more distinctive anatomic features than cellulitis. Lower extremity cellulitis or erysipelas is usually unilateral. Vesicles. (See "Orbital cellulitis" and "Septic dural sinus thrombosis". DIAGNOSIS — The diagnosis of cellulitis and erysipelas is based upon clinical manifestations. edema. Cellulitis and erysipelas manifest as areas of skin erythema. patients with cellulitis tend to have a more indolent course with development of localized symptoms over a few days' time. bullae. since the veins in this region are valveless (figure 1). Other forms of cellulitis include periorbital cellulitis. erysipelas lesions are raised above the level of surrounding skin. the areas around the eyes and nose) can be complicated by septic cavernous thrombosis.31]. patients with erysipelas tend to have acute onset of symptoms with systemic manifestations including fever and chills. abdominal wall cellulitis (in morbidly obese individuals). creating an appearance reminiscent of an orange peel texture ("peau d'orange"). and ecchymoses or petechiae may be observed. In addition. and there is a clear line of demarcation between involved and uninvolved tissue [29]. and management of diabetic infections of the lower extremities" and "Pseudomonas aeruginosa skin and soft tissue infections") ●Group B Streptococcus (see "Group B streptococcal infection in neonates and young infants". The lower extremities are the most common site of involvement for both cellulitis and erysipelas (picture 1A-B) [3. and warmth. They differ in that erysipelas involves the upper dermis and superficial lymphatics. since this region does not contain deeper dermis tissue. edema. and warmth. section on 'Other focal infection') CLINICAL MANIFESTATIONS — Cellulitis and erysipelas manifest as areas of skin erythema. buccal cellulitis (due to Streptococcus pneumoniae and. Rarely.34]. Laboratory findings may include leukocytosis and elevated inflammatory markers [35].) Additional manifestations of cellulitis and erysipelas include lymphangitis and inflammation of regional lymph nodes. Erysipelas has more distinctive anatomic features than cellulitis. . lymphedema. Edema surrounding the hair follicles may lead to dimpling in the skin. ●Erysipelothrix rhusiopathiae (see "Erysipelothrix infection") ●Cryptococcus neoformans (see "Fever and rash in immunocompromised patients without HIV infection") ●Helicobacter cinaedi (see "Fever and rash in HIV-infected patients") ●Pseudomonas aeruginosa (see "Fever and rash in immunocompromised patients without HIV infection" and "Clinical manifestations. and there is a clear line of demarcation between involved and uninvolved tissue. As a result. or lipodermatosclerosis. erysipelas lesions are raised above the level of surrounding skin. Haemophilus influenzae type b) and perianal cellulitis (due to group A beta-hemolytic Streptococcus) [33. Severe manifestations with systemic toxicity should prompt investigation for additional underlying sources of infection.32]. diagnosis. Crepitant and gangrenous cellulitis are unusual manifestations of cellulitis due to clostridia and other anaerobes. infections involving the medial third of the face (ie. Cellulitis may present with or without purulent drainage or exudate [30. bilateral involvement should prompt consideration of alternative causes including stasis dermatitis. Involvement of the ear (Milian's ear sign) is a distinguishing feature for erysipelas. Classic descriptions of erysipelas note "butterfly" involvement of the face.

46]. while culture of skin biopsy specimens yields a pathogen in 20 to 30 percent of cases [38. Blood cultures are positive in less than 5 percent of cases [36]. 45. Cultures of the interdigital spaces yielded beta-hemolytic streptococci. Clinical signs of soft tissue infection consist of local swelling and erythema followed by ecchymoses and sloughing of skin. special exposures (animal bite. Cultures of swabs from intact skin are not helpful and should not be performed. The affected area may be erythematous. respectively). (See 'Recurrent cellulitis' below. and skin biopsy are usually not necessary in the setting of mild infection [16. Gas gangrene can also be detected radiographically. 83 percent had tinea pedis. particularly in the setting of recent surgery or trauma. aureus. Radiographic examination can be useful to determine whether a skin abscess is present (via ultrasonography) and for distinguishing cellulitis from osteomyelitis (via magnetic resonance imaging) [48-51].37. radiographic imaging should not delay surgical intervention [52. needle aspiration. Culture results from needle aspiration vary from ≤5 to 40 percent [16. extensive skin involvement.36-44].43-45]. Pain out of proportion to exam findings may be observed. The presence of tissue crepitus favors clostridial infection. diabetes).Blood cultures. and 35 percent of cases. This was illustrated in a study of 24 patients with cellulitis.) Cellulitis must be distinguished from other infections including: .) Serology may have a useful diagnostic role in patients with recurrent cellulitis. and in patients with persistent systemic symptoms. underlying comorbidities (lymphedema.53]. Skin biopsy may be useful in cases of refractory cellulitis to evaluate for unusual pathogens or an alternative diagnosis. immunodeficiency. Radiographic examination cannot reliably distinguish cellulitis from necrotizing fasciitis or gas gangrene.39-42]. (See "Necrotizing soft tissue infections". ●Gas gangrene – Gas gangrene should be suspected in the setting of fever and severe pain in an extremity. neutropenia. and gram-negative bacilli (85. malignancy. Cultures of blood. Radiographic evaluation may be warranted in patients with underlying conditions such as diabetes. pus. (See "Necrotizing soft tissue infections" and "Clostridial myonecrosis". and/or bullae are warranted in the setting of systemic toxicity. water-associated injury). venous insufficiency or lymphedema. Fever is common. S. splenectomy.) ●Toxic shock syndrome – Toxic shock syndrome typically presents with pain that precedes physical findings. In addition. The diagnosis is established surgically with visualization of fascial planes. Cultures obtained from patients with lower extremity cellulitis and toe web intertrigo due to tinea pedis may be useful for identification of pathogenic bacteria [12]. warm and exquisitely tender.) DIFFERENTIAL DIAGNOSIS — Rapidly progressive erythema with signs of systemic toxicity should prompt consideration of severe infection. swollen. Patients may be normotensive on presentation but subsequently become hypotensive. (See "Clostridial myonecrosis". including: ●Necrotizing fasciitis – Necrotizing fasciitis is a deep infection that results in progressive destruction of the muscle fascia. molecular typing of isolates from paired blood and toe web cultures in two cases demonstrated identical streptococcal strains [47]. if there is clinical suspicion for these entities. or recurrent or persistent cellulitis [17.

●Skin abscess – Skin abscess is a collection of pus within the dermis and deeper skin tissues. often with central clearing and a necrotic center (picture 2 and picture 3). (See "Clinical manifestations and diagnosis of gout". and presence of tophi. Distinguishing cellulitis with and without bursitis depends on skilled palpation.) ●Osteomyelitis – Osteomyelitis may underlie an area of cellulitis. erythema. it consists of a region of erythema at the site of a tick bite. (See "Insect bites". stinging. bullae. which should demonstrate the characteristic urate crystals of gout or the calcium pyrophosphate crystals of pseudogout. The clinical suspicion can be substantiated by histopathologic examination of a skin biopsy. The diagnosis is suspected in a patient receiving drug treatment who presents with a rash of recent onset. (See "Skin abscesses. itching. and erythema. a local reaction is followed by a delayed skin reaction consisting of local swelling. it is a tender. and oozing. Clinical manifestations include joint pain. The rash is generally limited to one dermatome but can affect two or three neighboring dermatome. fluctuant. The diagnosis of septic arthritis is established based on synovial fluid examination. Clinical features include erythema. edema. (See "Septic bursitis". The diagnosis is established by polymerase chain reaction●Septic arthritis – Cellulitis may overlie a septic joint. and swelling overlying a single joint. and mild eosinophilia. The diagnosis is established based on serologic testing.) ●Erythema migrans – Erythema migrans is an early manifestation of Lyme disease. (See "Irritant contact dermatitis in adults". warmth. low-grade fever.) ●Acute gout – Acute gouty arthritis consists of severe pain. furuncles. or pain. and carbuncles". vesicles. (See "Overview of osteomyelitis in adults". which occurs as a result of damaged vessel walls.) ●Septic bursitis – Cellulitis may precede or accompany septic bursitis.) ●Insect bite – An insect bite triggers an inflammatory reaction at the site of the punctured skin. The diagnosis can be established by synovial fluid analysis. erythematous nodule that may present with surrounding cellulitic findings.) Noninfectious masqueraders of cellulitis include: ●Contact dermatitis – Contact dermatitis may be distinguished from cellulitis in that the contact dermatitis lesions are pruritic. which appears within minutes and consists of pruritic local erythema and edema. The reaction is generally limited to the site of contact and is associated with burning. warmth.) ●Drug reaction – A drug reaction presents with an erythematous maculopapular rash that involves the trunk and proximal extremities. A similar lesion may occur in patients with Southern tick–associated rash illness. The diagnosis is established by skin biopsy. It is prudent to pursue imaging for assessment of bone involvement in the setting of chronic soft tissue infection that fails to improve with appropriate antibiotic therapy.) . Radiographic imaging is warranted if septic bursitis is suspected. It may be accompanied by pruritus.) ●Vasculitis – The morphology of cutaneous lesions of vasculitis is variable. and limited range of motion. (See "Evaluation of adults with cutaneous lesions of vasculitis". Additional clues suggestive of gout include involvement of the first metatarsophalangeal joint. prior self-limited attacks of arthritis. although sensitivity in early disease is low. (See "Exanthematous (morbilliform) drug eruption". Macular and papular lesions are characteristically nonblanchable due to the presence of extravasated erythrocytes in the dermis. ●Herpes zoster – The rash of herpes zoster begins as erythematous papules that evolve into grouped vesicles (picture 4). In some cases. swelling. (See "Septic arthritis in adults".

Patients with edema may benefit from treatment with compressive stockings and diuretic therapy. cellulitis should be considered a manifestation of device infection if it originates on the skin directly overlying the prosthesis site) (algorithm 2). the evaluation consists of ultrasound evaluation. Parenteral therapy is also appropriate for patients with persistence or progression of symptoms despite 48 to 72 hours of appropriate oral therapy.) TREATMENT Nonantibiotic therapy — Management of cellulitis and erysipelas should include elevation of the affected area and treatment of underlying conditions. Lines should be drawn at the margin of erythema and a baseline digital image should be taken if possible. Attention to antibiotic dosing is important. The diagnosis is confirmed via biopsy. particularly in obese individuals. treatment should be directed at both the cellulitis and the predisposing condition. underlying conditions (such as diabetes). In such patients.) ●Panniculitis – Panniculitis refers to inflammation of subcutaneous fat and may have many causes. rapid progression of erythema. An infection involving purulence (whether the process began as an abscess [with secondary cellulitis] or as a cellulitis [with secondary purulence]) is potentially attributable to S. Many patients with cellulitis have underlying conditions that predispose them to developing recurrent cellulitis (these include tinea pedis. (See 'Purulent' below and 'Nonpurulent' below. (See "Clinical manifestations. Cellulitis in adults and children Clinical approach — Patients with mild cellulitis may be treated with oral antibiotics (algorithm 1). aureus. and/or proximity to an indwelling device (such as a prosthetic joint or a vascular graft. The skin should be sufficiently hydrated to avoid dryness and cracking without interdigital maceration. The approach to antibiotic selection for treatment of cellulitis depends on whether the clinical presentation consists of purulent or nonpurulent cellulitis. (See "Approach to the diagnosis and therapy of lower extremity deep vein thrombosis".) It is useful to document the baseline appearance of the physical findings at the start of antibiotic therapy. and special circumstances (such as animal bites and water exposure). which should be reflected in the choice of empiric antimicrobial therapy. Treatment with parenteral antibiotics is warranted for patients with signs of systemic toxicity. (See "Dermatophyte (tinea) infections" and "Medical management of lower extremity chronic venous disease" and "Clinical staging and conservative management of peripheral lymphedema". diagnosis. lymphedema. (See "Panniculitis: Recognition and diagnosis". Management of patients in these settings is discussed in detail separately. underdosing in obese patients (particularly those with morbid obesity and lymphedema) may result in higher rates of treatment failure [54]. immunocompromise. and chronic venous insufficiency). and management of diabetic infections of the lower extremities" and "Soft tissue infections due to dog and cat bites" and "Initial management of animal and human bites" and "Soft tissue infections following water exposure". ●Deep venous thrombosis – Findings suggestive of cellulitis involving the lower extremity should prompt consideration of deep venous thrombosis. both infectious and noninfectious (table 1).) .) Antibiotics — The following guidelines for empiric antimicrobial therapy should be modified as indicated in the setting of known pathogens. Elevation facilitates gravity drainage of edema and inflammatory substances.

Linezolid and tedizolid are additional agents with activity against MRSA. beta-hemolytic streptococci accounted for a much smaller proportion of these infections (2. this was illustrated in a randomized trial that included 524 patients with uncomplicated skin infections. they should be reserved for circumstances in which none of the other regimens listed cannot be used. careful monitoring is required. Options for empiric oral therapy of MRSA include (table 2 and table 3): ●Clindamycin ●Trimethoprim-sulfamethoxazole ●Tetracycline (doxycycline or minocycline) The efficacy of clindamycin and trimethoprim-sulfamethoxazole (TMP-SMX) for treatment of uncomplicated skin infection may be considered comparable. five days of therapy is appropriate for patients with uncomplicated cellulitis whose infection has improved within this time period [31. (See 'Diagnosis' above and 'Differential diagnosis' above. 17 percent). Patients with cellulitis typically have symptomatic improvement within 24 to 48 hours of beginning antimicrobial therapy.) Issues related to parenteral therapy for MRSA are discussed further separately. Purulent — Patients with purulent cellulitis (eg. aureus (MSSA.) The duration of therapy should be individualized depending on clinical response. section on 'Parenteral . pending culture results (algorithm 1 and algorithm 2) [30. This may be due to destruction of pathogens that release enzymes. In one study including 216 patients hospitalized with nonpurulent cellulitis. culture data should be reviewed carefully. In such cases. MRSA was the dominant organism. 90 percent of patients had improvement in clinical findings and serum C-reactive protein concentration three days after initiation of antimicrobial therapy [35.56].6 percent) [57]. respectively) [58]. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections".55]. isolated from 59 percent of patients.31]. In general. in the absence of a drainable abscess) should be managed with empiric therapy for infection due to MRSA. Extension of the duration (up to 14 days) may be warranted in the setting of severe infection and/or slow response to therapy. More than half of patients had residual inflammation at the end of therapy (median 11 to 15 days). Empiric therapy for infection due to beta-hemolytic streptococci is likely not necessary. and broadening antibiotic therapy to include coverage for gram-negative bacilli pending further diagnostic data is reasonable (algorithm 2). followed by methicillin-susceptible S. including both cellulitis and abscesses (cure rates for clindamycin and TMP-SMX were 80 and 78 percent. although visible improvement of clinical manifestations may take up to 72 hours. pursuit of radiographic evaluation for deeper infection is appropriate.A deepening of erythema may be observed following initiation of antimicrobial therapy. cellulitis associated with purulent drainage or exudate. In a study including 422 patients with purulent soft tissue infection. In addition. increasing local inflammation. (See "Pharmacology of antimicrobial agents for treatment of methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococcus". Persistence of erythema and/or systemic symptoms after this period of time should prompt consideration of resistant pathogens or alternative diagnoses. This should not be mistaken for a failure to respond to therapy. but relapse occurred in only 16 percent of these cases.

except for the mildest of cases. should be treated with parenteral therapy. Additional empiric coverage for MRSA is warranted in patients who do not respond to initial therapy.60-62].) Cellulitis in neonates — Treatment of cellulitis for neonates usually requires hospitalization and initial parenteral therapy. careful monitoring is required. Empiric parenteral therapy options include vancomycin plus either cefotaxime or gentamicin. aureus and other beta-hemolytic streptococci. cellulitis with no purulent drainage or exudate and no associated abscess) should be managed with empiric therapy for infection due to beta-hemolytic streptococci and MSSA [30]. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of skin and soft tissue infections". trimethoprim-sulfamethoxazole. Erysipelas — Patients with classic manifestations of erysipelas and systemic manifestations. section on 'Treatment approach'. options are summarized in the graphics (algorithm 1 and algorithm 2 and table 4). In addition. Antibiotics that should be avoided in this age group include tetracyclines. empiric coverage for MRSA should be considered in patients with risk factors for MRSA infection and in communities where the prevalence of MRSA is greater than 30 percent (table 5) [22. and ceftriaxone (cefotaxime is preferred over ceftriaxone).) Issues related to parenteral therapy for MRSA are discussed further separately.31. patients with recurrent infection in the setting of underlying predisposing conditions. such as fever and chills. section on 'Parenteral antibiotic therapy' and "Methicillin-resistant Staphylococcus aureus in children: Treatment of invasive infections". cure rates were comparable among those treated with cephalexin (for empiric treatment of beta-hemolytic streptococci and MSSA.) Nonpurulent — Patients with nonpurulent cellulitis (eg. 85 percent) [59]. Empiric therapy must include coverage for group B Streptococcus in addition to methicillin-resistant S. the efficacy of trimethoprim-sulfamethoxazole for treatment of uncomplicated skin infections (including cellulitis and abscesses) was comparable to that of clindamycin [58]. In addition. section on 'Treatment approach'. Therapy is usually administered for 7 to 10 days. they should be reserved for circumstances in which one of the other regimens listed cannot be used.antibiotic therapy' and "Methicillin-resistant Staphylococcus aureus in children: Treatment of invasive infections". Options for empiric oral therapy for treatment of both beta-hemolytic streptococci and MRSA include (table 6): ●Clindamycin ●Amoxicillin combined with trimethoprim-sulfamethoxazole ●Amoxicillin combined with a tetracycline (doxycycline or minocycline) Monotherapy with trimethoprim-sulfamethoxazole for treatment of nonpurulent cellulitis may be reasonable for patients with uncomplicated infection in the absence of systemic manifestations or comorbid conditions. Dosing is weight and age based (table 7). and patients with a previous episode of MRSA infection. patients with signs of systemic illness. (See "Pharmacology of antimicrobial agents for treatment of methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococcus". 82 percent) and those treated with cephalexin and trimethoprim- sulfamethoxazole (for empiric MRSA coverage. Appropriate choices . Linezolid and tedizolid are additional agents with activity against both beta-hemolytic streptococci and MRSA. This approach was illustrated in a randomized trial including 153 patients with cellulitis without abscess. in one study.

65]. options for prophylactic antibiotics include monthly or bimonthly (twice a month) intramuscular penicillin G benzathine injections (1. clindamycin. recurrences were observed in 17 percent of patients. In the setting of beta-lactam allergy.67]. attempting decolonization is reasonable. 5 to 10 days is usually appropriate. Cefazolin provides coverage against streptococci as well as MSSA. The duration of therapy should be individualized depending on clinical response. Alternatively. or the Streptozyme antibody assay [16]. cephalexin (if the patient can tolerate cephalosporins). ●For known or presumed staphylococcal infection. ●For known or presumed beta-hemolytic streptococcal infection. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Prevention and control". Ceftriaxone has activity against beta-hemolytic streptococci.63]. section on 'Decolonization' and "Methicillin-resistant Staphylococcus aureus in children: Prevention and control". if recurrent cellulitis occurs. the anti-deoxyribonuclease B test (anti-DNAse B). Assays include the anti-streptolysin O (ASO) reaction. 29 percent had recurrent infection [6. Patients with mild infection or those who have improved following initial treatment with parenteral antibiotic therapy may be treated with oral penicillin or amoxicillin (table 8). Anti-DNase B and AHT responses are more reliable than the ASO response following group A streptococcal skin infections. Staphylococcal prophylaxis for recurrent cellulitis is rarely necessary in children. the cause of erysipelas in the majority of cases. Early episodes of cellulitis cause lymphatic inflammation.) Infectious diseases consultation is warranted for patients with recurrent cellulitis despite antibiotic prophylaxis. or linezolid may be used [31]. RECURRENT CELLULITIS — Management of recurrent cellulitis can be a challenging problem.) Suppressive therapy may be continued for several months with interval assessments for tolerance to therapy.000 units for patients who weigh ≤27 kg) or oral therapy with penicillin V (250 to 500 mg orally twice daily) [64. this is discussed further separately.include ceftriaxone or cefazolin (table 8). the anti-hyaluronidase test (AHT). Supportive care with elevation . once-daily dosing allows for convenient outpatient administration. among 143 patients with erysipelas. 600.2 million units for patients who weigh >27 kg. (See 'Epidemiology' above. Support for the above approach comes from the following studies: ●In a study of 209 cases of cellulitis. Some clinicians favor serologic testing for beta-hemolytic streptococci to help guide the choice of suppressive antibiotic therapy. In patients with recurrent cellulitis due to S. and repeated infection can lead to lymphedema. Predisposing factors that can be alleviated should be addressed whenever possible [1]. aureus. Macrolides (particularly erythromycin) have also traditionally been used but may not be adequate therapy in areas with relatively high resistance rates among beta-hemolytic streptococci [31. patients may self-initiate antibiotic therapy when symptoms of infection begin and then seek medical attention immediately. the patient should be reevaluated promptly. which can be useful in settings where erysipelas cannot be reliably distinguished from cellulitis. In addition. We suggest administration of suppressive antibiotic therapy for patients with recurrent cellulitis. particularly in the setting of predisposing factors that cannot be alleviated (such as lymphedema and venous insufficiency). options for prophylactic antibiotics in adults include clindamycin (150 mg orally once daily) or trimethoprim-sulfamethoxazole (one double-strength tablet orally twice daily) [66].

easy-to-read materials.46. and edema (due to venous insufficiency).) ●Basics topics (see "Patient education: Cellulitis and erysipelas (skin infections) (The Basics)") ●Beyond the Basics topics (see "Patient education: Skin and soft tissue infection (cellulitis) (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS ●Cellulitis and erysipelas manifest as areas of skin erythema. (See 'Clinical manifestations' above. 95% CI 0. edema. erysipelas lesions are raised above the level of surrounding skin so that a clear line of demarcation between involved and uninvolved tissue is usually present. (See 'Clinical manifestations' above. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. These articles are best for patients who want a general overview and who prefer short. Findings from two of the included studies also demonstrated that antibiotic prophylaxis is cost-effective [69]. and warmth in the absence of underlying suppurative foci. and they answer the four or five key questions a patient might have about a given condition. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest. or lymphedema of the leg. Erysipelas has more distinctive anatomic features than cellulitis. Here are the patient education articles that are relevant to this topic. at the 5 th to 6th grade reading level. preexisting skin infection (such as impetigo or tinea pedis).79) [68].26-0.86. more sophisticated.55. Beyond the Basics patient education pieces are longer. “The Basics” and “Beyond the Basics. multiple previous episodes of cellulitis. (See "Society guideline links: Skin and soft tissue infections". inflammation (such as eczema or radiation therapy). A lower likelihood of response was observed among patients with a body mass index ≥33. of the affected area and treatment of underlying predisposing conditions are paramount. p = 0.) ●Predisposing factors include disruption to the skin barrier as a result of trauma (such as penetrating wounds or injection drug use).” The Basics patient education pieces are written in plain language. (See 'Nonantibiotic therapy' above and "Clinical staging and conservative management of peripheral lymphedema". and more detailed. penicillin (250 mg orally twice daily) nearly halved the risk of recurrence during 12 months of prophylaxis (hazard ratio 0. prophylactic antibiotic use reduced the risk of subsequent cellulitis (relative risk [RR] 0.) .01).) INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials.) ●In a systematic review and meta-analysis of five trials with a total of over 500 patients with at least one prior episode of cellulitis. SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. but the protective effect diminished rapidly after the prophylaxis period ended [64]. We encourage you to print or e-mail these topics to your patients. ●In a subsequent randomized trial that included 274 patients with two or more episodes of lower extremity cellulitis.35 to 0. These findings warrant further investigation since patients in these categories are most likely to receive long-term prophylaxis. 95% CI 0.

) ●Patients with mild cellulitis may be treated with oral antibiotics (algorithm 1). and F). and other pathogens include Staphylococcus aureus. (See 'Nonantibiotic therapy' above. aureus (MRSA) should be managed with empiric therapy for infection due to beta-hemolytic streptococci and MRSA.) .) ●Treatment of cellulitis for neonates usually requires initial parenteral therapy (table 8).) ●Patients with erysipelas and systemic manifestations (such as fever and chills) should be treated with parenteral therapy. Patients with mild infection or those who have improved following initial treatment with parenteral antibiotic therapy may be treated with oral therapy (table 8).) ●We suggest administration of suppressive antibiotic therapy for patients with recurrent cellulitis (Grade 2B). (See 'Microbiology' above.) ●Patients with purulent cellulitis (eg. In general. underlying comorbidities. Predisposing factors that can be alleviated should be addressed whenever possible. Parenteral therapy is also appropriate for patients with persistence or progression of symptoms despite 48 to 72 hours of appropriate oral therapy. Therapy is usually administered for 7 to 10 days. water-associated injury). Beta-hemolytic streptococci are the predominant cause of erysipelas.) ●The most common causes of cellulitis are beta-hemolytic Streptococcus (groups A. B. (See 'Cellulitis in neonates' above. special exposures (animal bite. (See 'Diagnosis' above. (See 'Cellulitis in adults and children' above. in the absence of a drainable abscess) should be managed with empiric therapy for infection due to MRSA. C. 5 days of therapy is appropriate for patients with uncomplicated cellulitis whose infection has improved within this time period. (See 'Purulent' above. (See 'Cellulitis in adults and children' above and 'Erysipelas' above. such as elevation of the affected area and treatment of underlying predisposing conditions. Extension of the duration (up to 14 days) may be warranted in the setting of severe infection and/or slow response to therapy. (See 'Nonpurulent' above. aureus (MSSA). (See 'Erysipelas' above. Cultures are necessary only in patients with systemic toxicity.●The diagnosis of cellulitis is based upon clinical manifestations. We recommend that patients with signs of systemic toxicity or erythema that has progressed rapidly should be treated initially with parenteral antibiotics (algorithm 2) (Grade 1B). Patients with nonpurulent cellulitis and additional risk factors for methicillin-resistant S.) ●Patients with nonpurulent cellulitis should be managed with empiric therapy for infection due to beta- hemolytic streptococci and methicillin-susceptible S.) ●Management of cellulitis and erysipelas should include supportive measures. or recurrent or persistent cellulitis. gram-negative aerobic bacilli are identified in a minority of cases.) ●The duration of therapy should be individualized depending on clinical response. cellulitis associated with purulent drainage or exudate. pending culture results (table 2). extensive skin involvement. G. (See 'Recurrent cellulitis' above.